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Clinical Review Science, medicine, and the future

Parkinson's disease

BMJ 1999; 318 doi: https://doi.org/10.1136/bmj.318.7179.311 (Published 30 January 1999) Cite this as: BMJ 1999;318:311
  1. A H V Schapira, professor of clinical neurosciences. (schapira@rfhsm.ac.uk)
  1. University Department of Clinical Neurosciences, Royal Free and University College Medical School and Institute of Neurology, University College London, London

    Parkinson's disease is the commonest neurodegenerative disease after Alzheimer's disease, with an estimated incidence of 20/100 000 and a prevalence of 150/100 000. It is characterised clinically by asymmetric onset of bradykinesia, rigidity, and, usually, resting tremor. The cause of the most common clinical features is the death of dopaminergic neurones in the substantia nigra of the midbrain. Lewy bodies are present in a proportion of surviving neurones. At the pathological level there is overlap with other neurodegenerative disorders including Alzheimer's disease, and this has been used to support the view that these diseases may share some common pathogenetic mechanisms.

    Parkinson's disease causes substantial morbidity and results in a shortened life span. It also has considerable economic consequences, including loss of earnings, cost of care, and cost of drug treatment (currently calculated at $1.1bn (£700m) worldwide). A major problem for researchers and clinicians is that, by the time patients' symptoms become sufficiently apparent for them to seek help, about 70-80% of their dopaminergic neurones may have already died. The length of the presymptomatic phase or incubation time of the disease may vary depending on the cause (fig 1). The main challenges in the treatment of Parkinson's disease are therefore (a) to protect dopaminergic neurones so that either the disease is prevented or its progression is slowed and (b) to provide treatment early to “rescue” neurones at risk.

    Aetiology and pathogenesis

    It is becoming clear that Parkinson's disease is probably not one disease but several with common clinical, pathological, and, possibly, biochemical end points. Although the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is the only environmental agent identified so far that is known to be capable of causing parkinsonism (and has done so within 14 days of exposure), other environmental factors such as use of pesticides and herbicides have been linked with an increased risk of disease. …

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